Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats

Chronic hypertension increases the risk of myocardial infarction and the morbidity and mortality associated with it. Although accelerated atherosclerosis is partially responsible, other abnormalities in the coronary circulation associated with hypertension, such as decreased coronary vascular capacity and capillary density, could also contribute. To evaluate the effects of these nonatherosclerotic abnormalities, we produced sudden coronary occlusion in nine chronically hypertensive dogs. The mean aortic pressure and left ventricular mass were about 50% greater in hypertensive dogs than in the nine controls. Before occlusion and 5 min and 49 h after occlusion, myocardial blood flow was measured with tracer microspheres. Also, the extent of infarction in selected myocardial segments was quantified histologically. We found that coronary occlusion reduced flows to a similar extent, and that, over a 48-h period, collateral flow increased to a similar extent in the two groups. In addition, the amount of necrosis associated with a given degree of ischemia was similar in the two groups. Although the extent of the left ventricle that became ischemic was greater in the hypertensive dogs (28 +/- 2 vs. 18 +/- 4%; P < 0.05), chronic hypertension and left ventricular hypertrophy did not limit the recruitment of collateral supply or increase the amount of necrosis associated with a given degree of ischemia.

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Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments

Frontiers in Physiology ◽

10.3389/fphys.2021.651246 ◽

2021 ◽

Vol 12 ◽

Author(s):

Carolina S. Cerrudo ◽

Susana Cavallero ◽

Martín Rodríguez Fermepín ◽

Germán E. González ◽

Martín Donato ◽

...

Keyword(s):

Gene Expression ◽

Left Ventricular Hypertrophy ◽

Cardiac Hypertrophy ◽

Ventricular Hypertrophy ◽

Pressure Overload ◽

Volume Overload ◽

Left Ventricular ◽

Prolonged Treatment ◽

Chronic Hypertension ◽

Peptide Profiles

The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.

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Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusion

Journal of the American College of Cardiology ◽

10.1016/0735-1097(89)90442-7 ◽

1989 ◽

Vol 14 (5) ◽

pp. 1365-1373 ◽

Cited By ~ 32

Author(s):

James B. Martins ◽

William Kim ◽

Melvin L. Marcus

Keyword(s):

Ventricular Tachycardia ◽

Coronary Artery ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Left Ventricular ◽

Chronic Hypertension ◽

Circumflex Coronary Artery ◽

Left Circumflex Coronary Artery

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Increased size of myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy.

Circulation Research ◽

10.1161/01.res.50.1.55 ◽

1982 ◽

Vol 50 (1) ◽

pp. 55-62 ◽

Cited By ~ 100

Author(s):

S Koyanagi ◽

C L Eastham ◽

D G Harrison ◽

M L Marcus

Keyword(s):

Myocardial Infarction ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Chronic Hypertension

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Left Ventricular Hypertrophy dan Fungsi Ginjal pada Penderita Hipertensi

Smart Medical Journal ◽

10.13057/smj.v1i2.28712 ◽

2018 ◽

Vol 1 (2) ◽

pp. 67

Author(s):

HERU SULASTOMO ◽

FADLAN AKHYAR FAUZI ◽

RATNA KUSUMAWATI

Keyword(s):

Uric Acid ◽

Left Ventricular Hypertrophy ◽

Kidney Function ◽

Ventricular Hypertrophy ◽

Case Control Study ◽

Blood Perfusion ◽

Left Ventricular ◽

Chronic Hypertension ◽

The Subject ◽

Control Study

Introduction: Chronic hypertension can cause complication such as left ventricular hypertrophy (LVH). LVH can lead renal artery vasoconstriction, impaire blood perfusion to glomerulus and change glomerulus filtration coeficient. The aim of this study was to compare kidney function between hypertensive patient with LVH and without LVH Methods: This was a case control study that conducted at Dr. Moewardi General Hospital Surakarta. All subjects has been diagnosed as hypertension more than 5 years. The diagnosis of LVH was based on electrocardiography (ECG) result. Kidney function was assessed based on serum ureum, creatinin, and uric acid levels. Results: The subject of this study was 26 hypertension patients with LVH and 13 hypertension patients without LVH. Serum ureum level in patients with LVH was higher than hypertension patients without LVH(24.92 ± 7.99 Vs 32.33±9.91, p= 0.004). Serum uric acid level in hypertension patients with LVH was higher compare to hypertension patients without LVH as well (5.26 ± 1.15 Vs 6.98 ± 1.83, p= 0.029). Whereas serum creatinine levels were not significantly different between two groups of subjects. Sulastomo et.al., Left Ventricular Hypertrophy dan Fungsi Ginjal pada Penderita Hipertensi Conclusion: : Serum ureum and uric acid levels in hypertensive subjects with LVH are higher than subjects without LVH. There is no difference between serum creatinin level in hypertensive subject with LVH and without LVH.

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The burden, correlates and outcomes of left ventricular hypertrophy among young Africans with first ever stroke in Tanzania

BMC Cardiovascular Disorders ◽

10.1186/s12872-021-02297-8 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Sarah Shali Matuja ◽

Patricia Munseri ◽

Candida Moshiro ◽

Khuzeima Khanbhai ◽

Karim Mahawish

Keyword(s):

Young Adults ◽

Left Ventricular Hypertrophy ◽

Brain Imaging ◽

Ventricular Hypertrophy ◽

Multivariable Analysis ◽

Left Ventricular ◽

Uncontrolled Hypertension ◽

Stroke Severity ◽

Chronic Hypertension ◽

Electrical Voltage

Abstract Background Left ventricular hypertrophy is a pathophysiological response often due to chronic uncontrolled hypertension. Our primary aim was to investigate the magnitude, correlates and outcomes of left ventricular hypertrophy as a surrogate maker for chronic uncontrolled hypertension in young adults ≤ 45 years with stroke. Our secondary aim was to determine the accuracy of electrocardiography using Sokolow-Lyon and Cornell criteria in detecting left ventricular hypertrophy compared to echocardiography. Methods This cohort study recruited young strokes who had undergone brain imaging, electrocardiography and transthoracic echocardiography at baseline. The modified Poisson regression model examined baseline correlates for left ventricular hypertrophy. The National Institute of Health Stroke Scale assessed stroke severity and the modified Rankin Scale assessed outcomes to 30-days. Performance of electrical voltage criterions was estimated using receiver operator characteristics. Results We enrolled 101 stroke participants. Brain imaging revealed ischemic strokes in 60 (59.4%) and those with intracerebral hemorrhage, 33 (86.8%) were localized to the basal ganglia. Left ventricular hypertrophy was present in 76 (75.3%:95%CI 65.7%–83.3%), and 30 (39.5%) and 28 (36.8%) had moderate or severe hypertrophy respectively. Young adults with premorbid or a new diagnosis of hypertension were more likely to have left ventricular hypertrophy, 47 (61.8%), and 26 (34.2%). On multivariable analysis, left ventricular hypertrophy was independently associated with not being on anti-hypertensive medications among hypertensives participants {adjusted risk ratio 1.4 (95%CI:1.04–1.94). The mean National Institute of Health Stroke score was 18 and 30-day mortality was 42 (43.3%). The sensitivity and specificity for Sokolow-Lyon in detecting left ventricular hypertrophy was 27% and 78%, and for Cornell was 32% and 52% respectively. Conclusions We identified a high proportion of left ventricular hypertrophy in young adults with stroke associated with chronic undertreated hypertension. While the study methodology does not allow us to determine causation, this association and knowledge of pathophysiological processes supports the notion that chronic hypertension is a major risk factor for young strokes associated with high mortality. Our findings did not support the use of the electrical voltage criteria for detecting left ventricular hypertrophy. We recommend low cost interventions like blood pressure screening and treatment to reduce this burden.

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